GLP1R and diabetes mellitus: According to their assumption, the reduction of the incretin effect in T2D patients is an epi-phenomenon of chronic hyperglycemia, irrespective of primary defects in GIP or GLP-1 action [24], which is consistent with the finding of loss of GIP insulinotropic efficacy in patients with diabetes of other etiologies, such as secondary to chronic pancreatitis, monogenic diabetes caused by HNF-1 alpha mutations, and autoimmune diabetes with preserved beta-cell function [25].